RAGE induces physiological activation of NADPH oxidase in neurons and astrocytes and neuroprotection

Author:

Seryogina Evgenia S.1,Kamynina Anna V.23,Koroev Dmitry O.3,Volpina Olga M.3,Vinokurov Andrey Y.1,Abramov Andrey Y.14ORCID

Affiliation:

1. Orel State University Russia

2. Research Center for Molecular Mechanisms of Aging and Age‐Related Diseases Moscow Institute of Physics and Technology (National Research University) Dolgoprudny Russia

3. Shemyakin‐Ovchinnikov Institute of Bioorganic Chemistry Russian Academy of Sciences Moscow Russia

4. Department of Clinical and Movement Neurosciences UCL Queen Square Institute of Neurology London UK

Abstract

The transmembrane receptor for advanced glycation end products (RAGE) is a signaling receptor for many damage‐ and pathogen‐associated molecules. Activation of RAGE is associated with inflammation and an increase in reactive oxygen species (ROS) production. Although several sources of ROS have been previously suggested, how RAGE induces ROS production is still unclear, considering the multiple targets of pathogen‐associated molecules. Here, using acute brain slices and primary co‐culture of cortical neurons and astrocytes, we investigated the effects of a range of synthetic peptides corresponding to the fragments of the RAGE V‐domain on redox signaling. We found that the synthetic fragment (60–76) of the RAGE V‐domain induces activation of ROS production in astrocytes and neurons from the primary co‐culture and acute brain slices. This effect occurred through activation of RAGE and could be blocked by a RAGE inhibitor. Activation of RAGE by the synthetic fragment stimulates ROS production in NADPH oxidase (NOX). This RAGE‐induced NOX activation produced only minor decreases in glutathione levels and increased the rate of lipid peroxidation, although it also reduced basal and β‐amyloid induced cell death in neurons and astrocytes. Thus, specific activation of RAGE induces redox signaling through NOX, which can be a part of a cell protective mechanism.

Funder

Russian Science Foundation

Publisher

Wiley

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